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89 Cards in this Set

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Where does plantar fasciitis pain originate?
At or near the site of the plantar fascia attachment to the medial tuberosity of the calcaneus
In what populations (age, activity) is plantar fasciitis most commonly seen?
* Peak between the ages of 40-60
* In younger populations of athletes esp runners, aerobic exercise dancers(!) and ballet dancers
What is thought to cause plantar fasciitis?
Repetitive microtrauma to the plantar fascia. Pathology of involved fascia usually reveals:
* degeneration of fibrous tissue
* with or without fibrobalst proliferation and
* chronic inflammation
Where is the plantar fascia & what is its function?
It's a thick fibrous band that starts at the medial tuberosity of the calcaneus,extends distally, dividing into 5 slips that insert into each metatarsal head. It tightens and elevates the longitudinal arch as well as inverting the hind foot during the push off phase of gait.
How do you diagnose plantar fasciitis?
Usually can be done on Hx and Ex alone, but imaging studies (xray, but bone scan more useful - shows uptake at attachment of plantar fascia to calcaneus).
What symptoms of plantar fasciitis are you looking for when taking a history?
* Inferior heel pain, severe with first steps upon rising in the morning or following inactivity during the day
* Pain usually lessens with weight bearing activity during the day, only to worsen wtih continued activity
* painful walking barefoot or up stairs
What physical signs of plantar fasciitis are you looking for on Ex?
Maximal tenderness elicited on plapation over the inferior heel, corresponding to the site of attachment of the plantar fascia.
What are some DDx for plantar fasciitis/heel pain?
* Calcaneal stress fractures
* Spondyloarthropathies
* RA
* Gou5t
* Neoplastic/infiltrative bone processes
* Nerve entrapment/compression
How do you treat plantar fasciitis?
* Ice, heat, massage, stretching of plantar fascia and calf muscles
* Orthotics/night splint
* foot strapping where appropriate
* Short course of NSAIDs where appropriate
* If necessary, local glucocorticoid injections
What are the key characteristic features of Rheumatoid Arthritis?
Persistent inflammatory synovitis, usually involving peripheral joints in a symmetric distribution, with potential to cause:
* cartilage damage
* bone erosions
* changes in joint integrity
What is the prevalence of RA?
Approx 1% of population (0.3-2.1%)
What are some risk factors for RA?
* Female (3x more common than in men)
* Age (80% develop the disease between 35-50)
* Genetic predisposition (4x the risk if you have a 1st degree relative with RA) - HLA - DR4
* Smoking in those with the HLA beta1 susceptibility allele
What causes RA?
It remains unknown. Some theorise that it is caused by an infectious agent, but that agent would have to be ubiquitous considering the worldwide distribution (like EBV or mycoplasma).
Describe the pathogenesis of RA (after the unknown insult...)
* Microvascular injury & increase in number of synovial lining cells (hypertrophic & hyperplastic)
* Perivascular infiltration with mononuclear cells
* Rheumatoid synovial cells express increased amounts of adhesion molecules
* Presence of both B cells & Tcells (majority CD4, but some CD8+)
* Antibodies to synovial tissue components (e.g. CCP)
* Activated mast cells
* Synovial fibroblasts activated (collagenase & cathepsins produced)
* Osteoclasts at sites of bony erosion
*
How does RA classically present?
* Prodrome (fatigue, anorexia, generalised weakness and vague MSK complaints)
* Several joints become affected in a symmetrical fashion
How might acute onset RA appear?
In about 10% of patients, onset is acute with:
* fever
* rapid development of polyarthritis
* lymphadenopathy
* splenomegaly
When is stiffness in RA most apparent?
After periods of inactivity. Morning stiffness for >1 hour duration is almost invariable features of inflammatory arthritis.
What constitutional symptoms may accompany RA?
* Weakness
* Easy fatiguability
* Weight loss
* Anorexia
What might you expect to see on examination of a joint with RA?
* Warmth
* Swelling
* Pain originating from the joint capsule (on stretching or distension).
Limitation of motion due to pain.
* Often the joint will be held in flexion to maximise joint volume & minimise distension of the capsule.
* Later: fibrous or bony ankylosis or soft tissue contractures lead to fixed deformities.

(Erythema is infrequent)
In which joints in the hand is RA most often seen?
It can affect any dairthrodial joint, but very commonly seen in:
* PIPs
* MCPs
* Wrists (almost always)
Distal interphalangeal joints are rarely involved.
Why should you check for carpal tunnel syndrome in RA patients?
Because synovitis of the wrist joints is a nearly uniform features of RA and may lead to median nerve entrapment (as well as limitation of motion & deformity)
Is the axial spine commonly involved in RA?
Usually limited to the upper cervical spine. Involvement of the lumbar spine is not seen, and lower back pain cannot be ascribed to RA (according to Harrisons)
What macroscopic changes occur in an RA joint over time?
1. Laxity of supporting tissue structures
2. Damage/weakening of ligaments, tendons & joint capsule
3. Cartilage degradation
4. Muscle imbalance
5. Unopposed physical forces associated with use of affected joints
What are some typical hand changes with RA?
1. Radial deviation at the wrist Unlar deviation of the digits, often with palmar subluxation of the proximal phalanges (Z deformity)
2. Hyperextension of the PIPs, with compensatory flexion of the DIPS) - swan neck
3. Flexion contracture of the PIPs & extension of the DIPs (boutonnieres)
4. Hyperextension of the 1st insterphalangeal joint & flexion of the first MCPs) - loss of thumb mobility & pinch
What are some of the extra-articular manifestations of RA?
* Rheumatoid nodules
* Clinical weakness and atrophy of skeletal muscle
* Rheumatoid vasculitis, which can potentially cause MI, & involve all organs
* pleuropulmonary manifestations: interstitial fibrosis, peluropulmonary nodules,pneumonitis & arteritis
Where can you find Rheumatoid nodules?
On periarticular strucutres, extensor surfaces or other areas subjected to mechanical pressure: commonly, on olecranon bursa, proximal ulna & Achilles tendon & occiput.

But also on pleura or meninges!!
What is Felty's Syndrome?
* Chronic RA and
* Splenomegaly and
* Neutropenia
On occasion, also:
* Anaemia
* Thrombocytopaenia.

Usually in pts with high titres of rheumatoid factor.
What's in rheumatoid nodules?
Central zone of necrotic material, a midzone of palisading macrophages (expressing HLA-DR antigens) and outer zone of granulation tissue).
What cancer is associated with RA?
Lymphoma (especially large B cell lymphoma).
What are some different causes of scoliosis?
1. Congenital (structural bony abnormality)
2. Neuromuscular (e.g. due to muscular dystrophy, cerebral palsy, polio, neurofibromatosis)
3. Idiopathic scoliosis (most common - there appears to be a genetic contribution to 'idiopathic' scoliosis)
How is idiopathic scoliosis classified?
* Age at time of onset (infantile, juvenile, adolescent, adult).
* Curvature according to side of convexity
What are the most common causative agents of infectious arthritis?
Staphylococcus aureus and Neisseria gonorrhoeae
What kind of infectious agent is more likely to cause subacute to chronic joint infection?
Mycobacterial or fungal infection
Which infectious agents can cause episodic inflammation?
Syphilis, Lyme disease, and the reactive arthritis that follows enteric infections and chlamydial urethritis.
Which chronic disease predisposes you to getting infections in more than one joint?
Rheumatoid arthritis.
What procedure should you perform in a case of suspected septic arthritis?
* Aspiration of the synovial fluid of the affected joint (if necessary, can use U/S guidance)
What synovial fluid findings might you expect with a bacterial infection?
Synovial cell counts averaging 100,000/L (range, 25,000–250,000/L), with >90% neutrophils
What synovial fluid findings might you expect in crystal-induced, rheumatoid, and other noninfectious inflammatory arthritides?
<30,000–50,000 cells/L (NB Normal synovial fluid contains <180 cells, predominantly mononuclear cells, per microliter)
How is bacterial septic arthritis treated?
* First take synovial fluid aspirate, & blood cultures
* Antibiotics (empiric, then directed by results of gram stain/cultures from synovial aspirate) - usually several weeks minimum (3 weeks for children, 4-6 weeks for adults)
* Drainage of pus with washout (repeated as clinically indicated) facilitates diffusion of antibiotic into the joint & may protect articular surface
What agent do you treat a case of suspected gonococcal arthritis with?
Cefotaxime or ceftriaxone
How does septic arthritis commonly present?
* >90% with a single affected joint
* Pain (uniform around the joint)
* Effusion
* Muscle spasm
* Fever (but not in some subgroups, e.g. RA or renal/hepatic insufficiency or pts with immunosuppression)
*
How does bacterial septic arthritis commonly present in an IVDU?
Infections of the spine, sacroiliac joints, or sternoclavicular joints
What changes might you expect to see on lab investigations (FBC, ESR, CRP)?
* Peripheral blood leucocytosis
* Raised ESR &/or CRP
What might you expect the synovial fluid to look like on aspiration of a bacterially septic joint?
Turbid, serosanguineous, or frankly purulent
How does a disseminated gonococcal infection present?
* Fever/chills
* Rash (papules, often on the trunk & extensor surfaces), which progress to hemorrhagic pustules)
* Migratory arthritis and tenosynovitis of hands, wrists, feet & ankles
* May be followed by true gonococcal arthritis (single infected joint)
What do you expect to find on synovial fluid stain and blood cultures in gonococcal arthritis?
* >50,000 leukocytes/L, can be obtained with ease
* gonococcus is only occasionally evident in gram-stained smears
* cultures of synovial fluid are positive in <40% of cases.
* Blood cultures are almost always negative.
Easier to obtain gonococcus from infected mucosal sites.
What is club foot (talipes equinovarus)?
Common congenital malformation where one or both feet are excessively plantar flexed, with the forefoot swung medially and the sole facing inward.
How is club foot classified?
1. congenital - affects the bones, muscles, tendons, and blood vessels of one or both feet
2. syndromic - associated with other deformities/chromosomal abnormalities (~10%)
3. positional - flexible, rather than rigid, and can be positioned into a neutral position easily by hand
Describe the abnormalities in anatomy that occur in club foot.
* mild to severe deformity of the talus, which is small and abnormal in all of its relationships.
* subluxation of the talo-calcaneo-navicular joint with under-development of the soft tissues on the medial side of the foot,
and frequently of the calf and perineal muscles.
* Shortening and fibrosis in the gastrocsoleus and its tendon, as well as in the posterior tibial muscle and tendon, also occur.
* The ligaments of the forefoot are normal, but the forefoot is adducted and supinated.
* Bony malposition and secondary contractures cause the foot to be held in a relatively fixed position, which is resistant to realignment.
Are club feet smaller, larger or the same size as the normal limb (if there is one)?
The clubfoot, calf, and leg are smaller and shorter than the normal limb.
What causes club foot?
80% of cases are idiopathic.
* intrinsic: early fetal onset of neurologic, muscular, or connective tissue disease with long-term implications for the neonate
* extrinsic: secondary to restriction to movement from multiple gestations, malpresentation, uterine cavity abnormalities.
What does the term torticollis refer to?
A clinical finding of a twisted or rotated neck
What is the most common type of congenital torticollis?
Congenital Muscular Torticollis. Often in babies in breech position.
When does congenital torticollis often become apparent?
By 2-4 weeks, after which time the child prefers to hold the head tilted to one side.
What are the clinical features of congenital torticollis?
* restriction of the range of motion of the neck, with the head tilted toward a shortened SCM and the chin rotated to the opposite side
* A characteristic mass may be palpable in the inferior one-third of the affected SCM. The mass, well-circumscribed and firm, is often referred to as the "pseudotumor" or "tumor" of the SCM.
What happens if you don't treat c.m. torticollis?
It may spontaneously resolve, or the child may develop a severe craniofacial abnormality.
How is C.M.Torticollis treated?
* Passive stretching
* Positioning & handling to encourage baby to develop the muscles on the affected side
* Surgery may be necessary if severe.
What can be some causes of acquired torticollis in children? Name 5.
Ijury or inflammation from a variety of conditions can cause spasm of cervical muscles or irritation of cervical nerves:

* minor trauma to the neck
* URTI
*retropharyngeal abscess
* vertebral subluxation
* spinal epidural hematomacervical lymphadenitis
* myositis
* retropharyngeal abscess
What should you be concerned about in a child with torticollis, plus stridor and/or drooling?
Retropharyngeal abcess or epiglottitis. Requires urgent evaulation.
In what populations are Colles fractures most prevalent?
1. Elderly osteoporotic patients who sustain a low energy fall (FOOSH: fall on an outstretched hand)
2. Young patients involved in sports who sustain a relatively high-energy fall
What is the classic deformity apparent with a colles' fracture?
Dinner fork deformity.
What should be examined in a patient with suspected Colles' fracture?
* Neurovascular status (incl sensory & motor fx of the median, radial & ulnar nerves)
* circulation (radial pulse, capillary refil of the nail beds)
* range of motion of wrist if possible
* check elbow & shoulder too
What is a Colles' fracture?
Distal radius fracture with DORSAL displacement of the distal radius fragment
What is a Smith's fracture?
Distal radius fracture with PALMAR displacement of the distal radius fragment
How do you manage a Colles/Smith's Fracture with neurovascualr compromise?
Immediate closed reduction of any displaced fracture should be performed, after providing analgesia, to attempt to alleviate symptoms. If persistent, emergency surgical referral.
How are Smiths Fractures managed?
Fractures with palmar displacement are commonly unstable and require orthopaedic referral.
How do you manage a Colles' fracture that is not significantly displaced (less than 20 degrees dorsally displaced)?
* Use a well molded surgical tong/double sugar tong splint (sounds noice) NOT a circumferential splint
* Analgesia as needed (NSAIDs and opioids may be used if appropriate)
* Ice frequently
* exercises/physio
* Adequate follow up
What are some symptoms of temporal (giant cell) arteritis?
* Headache of new onset
* tenderness or decreased pulse of the temporal artery
* Abrupt onset of visual disturbances
* Jaw claudication
* Symptoms of polymyalgia rheumatica
* Unexplained fever or anemia
* Fatigue, unexplained weight loss
* Elevated ESR and/or serum CRP
What is the gold standard for diagnosis of Giant Cell Arteritis?
Temporal artery biopsy (but don't wait for the biopsy to be scheduled/results to come back to start treatment!)

Resolution of the inflammatory infiltrate in GCA starts slowly, so you can still diagnose on biopsy taken several weeks after treatment is commenced.

(Other emerging options include MRI/angiography)
What is Giant Cell Arteritis?
A chronic vasculitis of medium and large vessels that occurs only in individuals older than 50 years of age
How is uncomplicated giant cell arteritis (that is, no signs of ischaemic organ damage) treated?
* With prednisone (start with 40-60mg dose, titrate up if not sufficient)
* with low-dose aspirin to prevent TIA/Stroke/ visual loss, and maybe a PPI in patients at risk of side effects of NSAIDs
What are some features of polymyalgia rheumatica?
Aching and morning stiffness in the
* shoulder and hip girdles
* neck
* torso
What are some AEs of Glucocorticosteroids relating to skin?
* purpura
* skin thinning
* striae
* skin cancers (SCC/BCC)
* steroid acne
* alopecia
* hypertrichosis
Describe Cushingoid appearance. Is the risk of Cushingoid dose and duration dependent?
Redistribution of body fat with:
* truncal obesity
* buffalo hump
* moon face

Yes. It is related to dose/duration (uptodate)
What are some Adverse Effects on the eye of Glucocorticosteroids?
* Cataracts
* Glaucoma (increased intraoccular pressure - usually in patients otherwised predisposed, e.g. Fam Hx)
* Central serous chorioretinopathy (oedema formation that can separate the retina from the choroid!)

Need to lower the dose of pred if these complications occur if at all possible.
What are some adverse effects of glucocorticoids on the cardiovascular system?
Increased risk of:
* MI
* heart failure
* stroke

* peripheral insulin resistance
* lipid abnormalities
What are some adverse effects of glucocorticosteroids on the gastrointestinal system?
* Ulcer formation
* Bleeding (less risk than that with NSAIDs - but be careful when the two are being used together! Think of prophylaxis)
* Gastritis
* Hepatic steatosis

ALSO: can mask serious GI disease
What fetal abnormality is associated with use of Glucocorticosteroids in pregnancy?
Cleft palate
What are some adverse effects of glucocorticosteroids on the musculoskeletal system?
* Osteoporosis
* osteonecrosis
* growth impairment in children
* proximal myopathy
What are some CNS/psychiatric AE's of glucocorticosteroids?
Initially, euphoria. However, with large doses, can develop:
* hypomanic symptoms
* depressive symptoms
* insomnia
* memory impairment
* akisthesia
* psychosis
What are 3 mechanisms by which glucocorticosteroids affect glucose metabolism?
1. Augments hepatic gluconeogenesis
2. Inhibits uptake of glucose into adipose tissue
3. Alteration of receptor & post-receptor function
In which patients can you assume there will be suppression of hypothalamic-pituitary-adrenal function?
Any patient:
* on more than 20 mg of prednisone a day for more than three weeks or
* who has clinical Cushing's syndrome
What can you do to minimise adverse effects of glucocorticoids?
* Have patient on lowest dose possible for the shortest period possible
* Use non-systemic GCS where possible, e.g. inhaled/topical/intra-articular
* Exercise to reduce mypoathy & osteoporosis
* Vit D, Calcium, Bisphosphonates for osteoporosis
* In postmenopausal women: estrogen therapy to minimize lumbar vertebral bone mineral loss
What factors affect absorption of glucocorticoids through the skin?
* location of application
* whether occlusive dressings are used (may increase absorption by 10 fold)
* What agent is used with it, e.g. salicylic acid & dimethylsulfoxide increase absorption
* Skin integrity (the more intact, the less it absorbs)
* Age of skin (infants & kids absorb more because their stratum corneum is thinner)
What are some adverse effects associated with paracetamol?
* rash, pruiritis (>5% children)
* May increase chloride, uric acid, glucose;
* may decrease sodium, bicarbonate, calcium (who would have thought?)
* Anaemia, neutropenia, leukopenia, pancytopenia
* Bilirubin increased, alkaline phosphatase increased
* nephropathy
* nausea, vomiting
* headache?!
What's a contraindication to use of paracetamol?
Severe hepatic impairment
To which patients should you be cautious re use/recommendation of paracetamol?
* Chronic malnutrition
* Alcoholics
* G6PD deficiency: hemolysis may occur
* hepatic impairment
* severe renal impairment
What is the maximum daily dose of paracetamol?
4g/day.
What might paracetamol do when taken with Vitamin K Antagonists?
Increase their anticoagulant effects. Monitor.